Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury

K. Soejima, F. C. Schmalstieg, L. D. Traber, Csaba Szabo, A. Salzman, D. L. Traber

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

This study tested the hypothesis that nitric oxide (NO) synthesized from inducible NO synthase (iNOS) is responsible for the cardiac dysfunction observed after burn and smoke inhalation injury. Twelve sheep received 40% third-degree burn and smoke inhalation under halothane anesthesia. The animals were divided into two groups: a MEG group [iNOS was inhibited with mercaptoethylguanidine (MEG), a selective inhibitor of iNOS, n=6] and a control group (n=6). The control group showed a significant increase in NO2 -/NO3 - (NOx) concentration, metabolite of NO, in plasma after 24 h, whereas the MEG group did not. In the control group, cardiac depression was observed immediately after injury associated with hemoconcentration. Cardiac function returned to a normal level within 6 h following injury. In the control group cardiac dysfunction was observed again after 24 h although the hemoconcentration peaked at 24 h after injury and then began to resolve. In the MEG group, cardiac depression and hemoconcentration were not observed. The present data suggest that cardiac depression seen with this combination injury consists of two phases and that the later phase is mediated by iNOS-NO.

Original languageEnglish (US)
Pages (from-to)809-815
Number of pages7
JournalBurns
Volume27
Issue number8
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Smoke Inhalation Injury
Nitric Oxide
Nitric Oxide Synthase
Control Groups
Wounds and Injuries
Nitric Oxide Synthase Type II
Inhalation Burns
Halothane
Smoke
Sheep
Anesthesia
2-mercaptoethylguanidine

Keywords

  • Inducible nitric oxide synthase
  • Inflammatory cytokine
  • Mercaptoethylguanidine
  • Peroxynitrite
  • Vascular hyperpermeability

ASJC Scopus subject areas

  • Emergency Medicine
  • Surgery

Cite this

Soejima, K., Schmalstieg, F. C., Traber, L. D., Szabo, C., Salzman, A., & Traber, D. L. (2001). Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury. Burns, 27(8), 809-815. https://doi.org/10.1016/S0305-4179(01)00051-1

Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury. / Soejima, K.; Schmalstieg, F. C.; Traber, L. D.; Szabo, Csaba; Salzman, A.; Traber, D. L.

In: Burns, Vol. 27, No. 8, 2001, p. 809-815.

Research output: Contribution to journalArticle

Soejima, K, Schmalstieg, FC, Traber, LD, Szabo, C, Salzman, A & Traber, DL 2001, 'Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury', Burns, vol. 27, no. 8, pp. 809-815. https://doi.org/10.1016/S0305-4179(01)00051-1
Soejima, K. ; Schmalstieg, F. C. ; Traber, L. D. ; Szabo, Csaba ; Salzman, A. ; Traber, D. L. / Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury. In: Burns. 2001 ; Vol. 27, No. 8. pp. 809-815.
@article{dac8aca90b954483a07513288fcbdc28,
title = "Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury",
abstract = "This study tested the hypothesis that nitric oxide (NO) synthesized from inducible NO synthase (iNOS) is responsible for the cardiac dysfunction observed after burn and smoke inhalation injury. Twelve sheep received 40{\%} third-degree burn and smoke inhalation under halothane anesthesia. The animals were divided into two groups: a MEG group [iNOS was inhibited with mercaptoethylguanidine (MEG), a selective inhibitor of iNOS, n=6] and a control group (n=6). The control group showed a significant increase in NO2 -/NO3 - (NOx) concentration, metabolite of NO, in plasma after 24 h, whereas the MEG group did not. In the control group, cardiac depression was observed immediately after injury associated with hemoconcentration. Cardiac function returned to a normal level within 6 h following injury. In the control group cardiac dysfunction was observed again after 24 h although the hemoconcentration peaked at 24 h after injury and then began to resolve. In the MEG group, cardiac depression and hemoconcentration were not observed. The present data suggest that cardiac depression seen with this combination injury consists of two phases and that the later phase is mediated by iNOS-NO.",
keywords = "Inducible nitric oxide synthase, Inflammatory cytokine, Mercaptoethylguanidine, Peroxynitrite, Vascular hyperpermeability",
author = "K. Soejima and Schmalstieg, {F. C.} and Traber, {L. D.} and Csaba Szabo and A. Salzman and Traber, {D. L.}",
year = "2001",
doi = "10.1016/S0305-4179(01)00051-1",
language = "English (US)",
volume = "27",
pages = "809--815",
journal = "Burns",
issn = "0305-4179",
publisher = "Elsevier Limited",
number = "8",

}

TY - JOUR

T1 - Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury

AU - Soejima, K.

AU - Schmalstieg, F. C.

AU - Traber, L. D.

AU - Szabo, Csaba

AU - Salzman, A.

AU - Traber, D. L.

PY - 2001

Y1 - 2001

N2 - This study tested the hypothesis that nitric oxide (NO) synthesized from inducible NO synthase (iNOS) is responsible for the cardiac dysfunction observed after burn and smoke inhalation injury. Twelve sheep received 40% third-degree burn and smoke inhalation under halothane anesthesia. The animals were divided into two groups: a MEG group [iNOS was inhibited with mercaptoethylguanidine (MEG), a selective inhibitor of iNOS, n=6] and a control group (n=6). The control group showed a significant increase in NO2 -/NO3 - (NOx) concentration, metabolite of NO, in plasma after 24 h, whereas the MEG group did not. In the control group, cardiac depression was observed immediately after injury associated with hemoconcentration. Cardiac function returned to a normal level within 6 h following injury. In the control group cardiac dysfunction was observed again after 24 h although the hemoconcentration peaked at 24 h after injury and then began to resolve. In the MEG group, cardiac depression and hemoconcentration were not observed. The present data suggest that cardiac depression seen with this combination injury consists of two phases and that the later phase is mediated by iNOS-NO.

AB - This study tested the hypothesis that nitric oxide (NO) synthesized from inducible NO synthase (iNOS) is responsible for the cardiac dysfunction observed after burn and smoke inhalation injury. Twelve sheep received 40% third-degree burn and smoke inhalation under halothane anesthesia. The animals were divided into two groups: a MEG group [iNOS was inhibited with mercaptoethylguanidine (MEG), a selective inhibitor of iNOS, n=6] and a control group (n=6). The control group showed a significant increase in NO2 -/NO3 - (NOx) concentration, metabolite of NO, in plasma after 24 h, whereas the MEG group did not. In the control group, cardiac depression was observed immediately after injury associated with hemoconcentration. Cardiac function returned to a normal level within 6 h following injury. In the control group cardiac dysfunction was observed again after 24 h although the hemoconcentration peaked at 24 h after injury and then began to resolve. In the MEG group, cardiac depression and hemoconcentration were not observed. The present data suggest that cardiac depression seen with this combination injury consists of two phases and that the later phase is mediated by iNOS-NO.

KW - Inducible nitric oxide synthase

KW - Inflammatory cytokine

KW - Mercaptoethylguanidine

KW - Peroxynitrite

KW - Vascular hyperpermeability

UR - http://www.scopus.com/inward/record.url?scp=0035160335&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035160335&partnerID=8YFLogxK

U2 - 10.1016/S0305-4179(01)00051-1

DO - 10.1016/S0305-4179(01)00051-1

M3 - Article

VL - 27

SP - 809

EP - 815

JO - Burns

JF - Burns

SN - 0305-4179

IS - 8

ER -